scholarly journals Nitric oxide produced by periostial hemocytes modulates the bacterial infection-induced reduction of the mosquito heart rate

2020 ◽  
Vol 223 (15) ◽  
pp. jeb225821
Author(s):  
Tania Y. Estévez-Lao ◽  
Leah T. Sigle ◽  
Scherly N. Gomez ◽  
Julián F. Hillyer
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Nitric Oxide Synthase ◽  
Bacterial Infection ◽  
Micrococcus Luteus ◽  
Cardiac Phenotype ◽  
Expression Of Genes ◽  
Genes Encoding ◽  
Neuropeptide F ◽  
Oxide Synthase

ABSTRACTThe circulatory and immune systems of mosquitoes are functionally integrated. An infection induces the migration of hemocytes to the dorsal vessel, and specifically, to the regions surrounding the ostia of the heart. These periostial hemocytes phagocytose pathogens in the areas of the hemocoel that experience the highest hemolymph flow. Here, we investigated whether a bacterial infection affects cardiac rhythmicity in the African malaria mosquito, Anopheles gambiae. We discovered that infection with Escherichia coli, Staphylococcus aureus and Staphylococcus epidermidis, but not Micrococcus luteus, reduces the mosquito heart rate and alters the proportional directionality of heart contractions. Infection does not alter the expression of genes encoding crustacean cardioactive peptide (CCAP), FMRFamide, corazonin, neuropeptide F or short neuropeptide F, indicating that they do not drive the cardiac phenotype. Infection upregulates the transcription of two superoxide dismutase (SOD) genes, catalase and a glutathione peroxidase, but dramatically induces upregulation of nitric oxide synthase (NOS) in both the heart and hemocytes. Within the heart, nitric oxide synthase is produced by periostial hemocytes, and chemically inhibiting the production of nitric oxide using l-NAME reverses the infection-induced cardiac phenotype. Finally, infection induces the upregulation of two lysozyme genes in the heart and other tissues, and treating mosquitoes with lysozyme reduces the heart rate in a manner reminiscent of the infection phenotype. These data demonstrate an exciting new facet of the integration between the immune and circulatory systems of insects, whereby a hemocyte-produced factor with immune activity, namely nitric oxide, modulates heart physiology.

scholarly journals Enteric descending and afferent neural signaling stimulated by giant migrating contractions: essential contributing factors to visceral pain

2007 ◽  
Vol 292 (2) ◽  
pp. G572-G581 ◽  
Author(s):  
Sushil K. Sarna
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Nitric Oxide Synthase ◽  
Muscarinic Receptors ◽  
Visceral Pain ◽  
Intestinal Segment ◽  
Descending Inhibition ◽  
Oxide Synthase ◽  
Stimulation Of ◽  
Giant Migrating Contractions

We investigated whether strong compression of an intestinal segment by giant migrating contractions (GMCs) initiates pseudoaffective signals from the gut, similar to those initiated by its distension with a balloon. The experiments were performed on conscious dogs by using close intra-arterial infusions of test substances that affect the receptors only in the infused segment. The stimulation of GMCs by close intra-arterial infusion of CGRP or distension of an intestinal segment by balloon increased the heart rate; the increase in heart rate was greater when the balloon distension and GMCs occurred concurrently in separate intestinal segments. The suppression of contractility in the distended segment blocked the increase in heart rate. By contrast, the stimulation of rhythmic phasic contractions (RPCs) or their spontaneous occurrence did not increase the heart rate. The occurrence of GMCs as well as intestinal distension also produced descending inhibition. The descending inhibition was blocked by the inhibition of nitric oxide synthase, but it was unaffected by the inhibition of adenylyl cyclase, purinergic receptors P2X and P2Y, and muscarinic receptors M1 and M2. The synaptic transmission for descending inhibition was mediated primarily by nicotinic receptors and activation of nitric oxide synthase. It was unaffected by the inhibition of tachykinin receptors NK1, NK2, and NK3; serotonin receptors 5-HT1A, 5-HT2/5-HT1C, 5-HT3, and 5-HT4; and muscarinic receptors. Our findings show that GMCs, but not RPCs, initiate pseudoaffective signals from the gut. In the presence of visceral hypersensitivity or impaired descending inhibition, the GMCs may become a noxious stimulus.

Variation of genes involved in oxidative and nitrosative stresses in depression

2018 ◽  
Vol 48 (1) ◽  
pp. 38-48 ◽  
Author(s):  
Paulina Wigner ◽  
Piotr Czarny ◽  
Ewelina Synowiec ◽  
Micha� Bijak ◽  
Katarzyna Białek ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Depressive Disorders ◽  
Nitrosative Stress ◽  
Nucleotide Polymorphisms ◽  
Oxidative And Nitrosative Stress ◽  
Increased Risk ◽  
Genes Encoding ◽  
Oxide Synthase ◽  
The Impact

AbstractThe dominating hypothesis among numerous hypotheses explaining the pathogenesis of depressive disorders (DD) is the one involving oxidative and nitrosative stress. In this study, we examined the association between single-nucleotide polymorphisms of the genes encoding SOD2 (superoxide dismutase 2), CAT (catalase), GPx4 (glutathione peroxidase 4), NOS1 (nitric oxide synthase 1), NOS2 (nitric oxide synthase 2), and the development of depressive disorders. Our study was carried out on the DNA isolated from peripheral blood collected from 281 depressed patients and 229 controls. Using TaqMan probes, we genotyped the following six polymorphisms: c.47T > C (p.Val16Ala) (rs4880) in SOD2, c.-89A > T (rs7943316) in CAT, c.660T > C (rs713041) in GPx4, c.-420-34221G > A (rs1879417) in NOS1, c.1823C > T (p.Ser608Leu) (rs2297518), and c.-227G > C (rs10459953) in NOS2. We found that the T/T genotype of the c.47T > C polymorphism was linked with an increased risk of depression. Moreover, the T/T genotype and T allele of c.660T > C increased the risk of DD occurrence, while the heterozygote and C allele decreased this risk. On the other hand, we discovered that the A/A genotype of c.-89A > T SNP was associated with a reduced risk of DD, while the A/T genotype increased this risk. We did not find any correlation between the genotypes/alleles of c.-420-34221G > A, c.1823C > T, and c.-227G > C, and the occurrence of DD. In addition, gene-gene and haplotype analyses revealed that combined genotypes and haplotypes were connected with the disease. Moreover, we found that sex influenced the impact of some SNPs on the risk of depression. Concluding, the studied polymorphisms of SOD2, CAT and GPx4 may modulate the risk of depression. These results support the hypothesis that oxidative and nitrosative stresses are involved in the pathogenesis of depressive disorders.

scholarly journals Altered responses to bacterial infection and endotoxic shock in mice lacking inducible nitric oxide synthase

Cell ◽  
1995 ◽  
Vol 81 (4) ◽  
pp. 641-650 ◽  
Author(s):  
John D. MacMicking ◽  
Carl Nathan ◽  
Gary Hom ◽  
Nicole Chartrain ◽  
Daniel S. Fletcher ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Bacterial Infection ◽  
Inducible Nitric Oxide Synthase ◽  
Endotoxic Shock ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

scholarly journals Impaired regulation of neuronal nitric oxide synthase and heart rate during exercise in mice lacking onenNOSallele

2004 ◽  
Vol 558 (3) ◽  
pp. 963-974 ◽  
Author(s):  
E. J. F. Danson ◽  
K. S. Mankia ◽  
S. Golding ◽  
T. Dawson ◽  
L. Everatt ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Nitric Oxide Synthase ◽  
Neuronal Nitric Oxide Synthase ◽  
Oxide Synthase
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